Bone modelling processes at the endosteal surface of human femora. Scanning electron microscopical studies in normal bone and in renal osteodystrophy
- PMID: 157599
- DOI: 10.1007/BF01102742
Bone modelling processes at the endosteal surface of human femora. Scanning electron microscopical studies in normal bone and in renal osteodystrophy
Abstract
In femoral bone of 10 adult patients without bone disease and of 15 patients with secondary hyperparathyroidism, thy after nonmineralised organic material had been removed from the endosteal surface by sodium hypochlorite. This technique permits one to analyse the effects of past osteoblastic and osteoclastic activities. Im normal bone, the endosteal envelope shows a highly ordered texture: The main part of the inner surface is represented by fully mineralised smooth surfaces without evidence of apposition or resorption (so called neutral surfaces). In apposition areas, collagen fibers are still incompletely mineralised. Ordered mineral deposits are observed, consisting of spindleshaped calcospherites of uniform size. The resorption areas are sharply delimited. The resorption layer shows a small difference of level with respect to the surrounding neutral surface. Resorption areas consist of numerous lacunae with a smooth bottom. Individual lacunae are encircled by shallow ridges which run almost perpendicularly to the main direction of collagen fibers that have been exposed by resorption. These findings suggest that in normal bone osteoclasts act as a corrdinated group of cells. The direction of advance of the resorption area is to some extent influenced by the collagen pattern of bone. In patients with secondary hyperparathyroidism, domain formation of the endosteal surface can no longer be recognized. The size and shape of caleospherites are extremely heterogeneous, a finding interpreted as evidence of formation of woven bone. Resorption areas are irregularly determined and often resemble worm-eaten wood. The planes of resorption vary in direction and depth and in general resorption cavities penetrate deeper than in normal bone. These findings point to loss of coordinated cell action under the influence of hyperparathyroidism. The observations suggest that in hyperparathyroidism endosteal cells do not respond to local factors which influence endosteal cell activities in modelling processes of normal bone. Such local factors consist of the pattern of collagen andlamellar organisation on one hand and mechanical forces presumably via pizo-electrical potentials, on the other. In hyperparathyroidism the interdependence between bone matrix texture and spatial orientation of bone surface lining cell activities is lost.
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